The late Dr. John Richardson was a family physician who practiced in Newcastle, UK. For more than 40 years, Dr. Richardson tracked his patients, taking detailed histories, documenting their illnesses, and performing autopsies on those who died. These records provided the basis for his book, Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies, which is regarded as one of the most valuable medical compilations in the field of ME/CFS.

Early in his practice, Dr. Richardson realized that enteroviral infections were endemic among his patients, and that not only did they spread from one family to another, they were transmitted from one generation to the next. Out of 7000 patients who contracted viral illnesses, 1780 went on to develop pathologies - 894 had subsequent organ pathology and 111 died. The causes of death were cardiac failure, carcinomas, and other organ failure.

While all of these deaths were attributed to their proximate causes (heart attack, cancer, etc.) Dr. Richardson showed, through autopsy results, that the underlying pathology was caused by enteroviruses, which were still live and replicating in the affected organs years after the initial infection had resolved.

Dr. Richardson noted that roughly 20% of those affected by enteroviral infections (primarily coxsakie virus) developed ME. Because of his diligence, knowledge, and powers of observation, Dr. Richardson soon became one of the world's foremost experts in the disease.

Dr. Richardson's book is not designed for the layperson, which makes for difficult reading. But the information it contains is worth the effort. Below is the section on diagnosing ME, excerpted from Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies, CRC Press; 1st edition (August 15, 2001).

One can only hope that Drs. Cheney, Peterson, Bell and other physicians who have assembled years of data from thousands of ME/CFS patients will undertake to make their observations and clinical data available to the public, as Dr. Richardson has done.

You can find links to Dr. Richardson's papers and presentations here.__________________________________________

MYALG1C ENCEPHALOMYELITIS

Nowhere is a variety of systemic symptoms seen more often than in myalgic encephalomyelitis. While it is a defined entity, other organ pathology is not infrequent and can obscure the picture. In this series about 25 percent also developed other antibodies, and antithyroid an­tibodies occurred in about 20 percent of cases. A lecture given at Cambridge in 1990 summarizes this syndrome (Nightingale Re­search Foundation, 1991).

Much has been written on the subject. It has been treated as a myth, or as a single entity that was then claimed by some to be psychiatric or by others to be organic in origin. In the first group, labels were ap­plied ranging from depression to hysteria while in the second, valid observation as well as vague hypotheses are still the order of the day. This merely illustrates the limitations of the medical mind in fully ex­plaining the fundamental pathology of all illness.

The observations in the following sections are the result of contin­uous follow-up and analysis of sequential illness in patients varying in situation and time over a period of forty years.

Prevalence and Clinical Diagnosis

As with poliomyelitis, surveys have shown ME to be epidemic, endemic, and also sporadic. It may follow an acute viral illness such as Bornholm disease, pericarditis, labyrinthitis, or meningoencephalitis. A more vague flulike illness with chest or bowel disturbance may be the harbinger of a more insidious onset. Apparent malaise not only fails to end but becomes more defined, developing symptoms such as anomia or severe concentration difficulty in a previously highly accomplished person who now cannot recall a paragraph even after reading it several times. Muscle power may not appear to be affected, but if examined carefully, softened and very tender areas may be demonstrated. Muscle jitter is a feature in 25 percent of these cases.

This can be shown by seating the patient on the examination table and asking him or her to raise and lower the lower leg, whereby the jitter is easily seen. Concomitant myocardial or endocrine gland dysfunction also occurs, but if these resolve, the physician may be very frustrated to find that the patient is still ill. The graphs in Figure 3.12 show relative prevalence, and it is apparent that females do not predominate as some have thought, given the overall CNS sequelae to viral illness. Since these graphs were developed, the absolute number of cases being considered has risen, but the percentages have remained unchanged.

I devised the scoring chart shown in Table 3.3 in the early 1960s to summarize the symptoms that were recorded by patients in their own written histories of this illness. There were approximately 300 such written histories, and the symptoms that form the basis of this chart occurred in 80 percent of the cases.

If the patient qualifies for the diagnosis for each question, then the score indicated in the third column is recorded in the fourth column. The sum of the values in this fourth column then represents the patient's overall score.

Table 3.3 ME scoring chart

1. Has there ever been any evidence, either illness or titer, of past viral infection? 1

2. FATIGUE: (a) Are you less than 33% efficient per full day (including hobbies after work, etc.) 2

(b) Do you need a period of bed or settee rest: during each day, or 3 on 2 or 3 days a week? 2

3. Have you excessive fatigue after work effort? 2

4. Do you have nocturnal sweats or cold feelings? 2

5. EVIDENCE OF DISTURBED MENTAL ACTIVITY

(a) Do you have difficulty finding the correct words? 1

(b) Can you write a long letter without your handwriting deteriorating? 1

(c) Do you tire if you have to talk for long? 1

6. FAINT ATTACKS (VASOMOTOR CNS INSTABILITY)

(a) Do you tend to have faint attacks:and lose consciousness? 3or: without loss of consciousness but have to sit down or lie down? 2

7. Do you feel fatigued on waking? 1

8. Can you stand a lot of “chatter” (hyperacusis)? 1

9. Do you have cold or numb feelings in your extremities of face? 2

10. Is your gait consistent with your age or is it that of a person much older or unsteady? 1

Answering these questions, therefore, yields a global view of the symptoms that occur in ME. An overall score of fifteen or more is highly suggestive of the condition and can be broken down into four sections:

1. Fatigue. This can be either central fatigue or muscle fatigue. Central fatigue is probed in question 7 while peripheral fatigue is indicated by questions 3 and 10. The resulting combination would be suggested by question 2 (a) and (b). Muscle fatigue is known to be related to an excess of lactic acid after work effort. In this condition, however, excessive activity is usually reflected the following day, and it may take days for the patient to recover.

2. Mental Activity. Question 5(a) indicates anomia, which is a very well recognized symptom in this condition, while question 5(b) reflects the motor fatigue involved in transposing verbal to written language. This may indicate the involvement of supra- and infrasensorial mechanisms within the brain and may also be evidenced by a positive response to question 5(c).

3. CNS Instability. This is seen in varying degrees of severity in 80 percent of the cases, hence the two grades of response to question 6(a). The test for the former is performed by placing the patient prone on the examination couch and performing serial ECGs and carefully monitoring blood pressure. The backrest is then raised to 45° and blood pressure recorded at two-minute intervals. If any change in heart rate is detected, then further ECGs are performed. After five minutes the patient is asked to stand upright, and further blood pressures are recorded. In only 10 percent of cases is there a significant change in heart rate, but changes in blood pressure as indicated usually occur. In the supine position, the blood pressure normally is quite low but in the 45° position often rises by 50 mm systolic and 20 mm diastolic. When the patient assumes the erect position it again falls to levels either equal to or below those recorded for the supine position. Only in the small minority of cases with a concomitant bradycardia did a collapse occur, but, as indicated, many of the other patients felt weak and had to sit down.

Question 8 again alludes to the central fatigue in which the patient has a limited ability to absorb information. On occasion, certain tones become extremely painful, constituting the "tensor tympani" syndrome.

Question 9 relates to vasomotor instability reflected in temperature or sensory changes, which again may reflect abnormal reception in the hypothalamic nuclei.

4. Overall Result. Finally, question 10 is obviously the result of a conglomeration of the other symptoms.

The Differential Diagnosis of Myalgic Encephalomyelitis

Obviously the history obtained is of first importance. In the cases so far, it is striking how consistent the symptoms are that characterize this condition. Moreover, when the cases are studied in retrospect, the following fact emerges. Approximately 7,000 cases of viral illness over four decades have been listed and broken down into five groups. The first contained over 5,000 cases who had had quite a severe ill­ness but recovered without sequelae within six months. However, just under 20 percent of this group did have a recurrence of enteroviral or­igin at a future date but not always with the same syndrome, e.g., one case had Bornholm disease and the second attack was viral meningi­tis. These were chiefly enteroviral cases, and it is interesting that no one in Group 1 progressed to postviral illness, be it ME or another syndrome. However, of all 7,000 cases, 1,670 did have postviral syn­dromes, some from the original attack and some who had a recurrent illness (Group 2).

It is of interest to note that some of the initial illnesses appeared to clear completely (e.g., meningitis or Bornholm disease), while others (e.g., pericarditis, myocarditis, nephritis, etc.), could remit or pursue a more chronic course. A lifelong syndrome (e.g., diabetes) might en­sue in a small minority. Yet again, in a small minority with acute on­set there are those who do not make a recovery and develop ME. The difficulty of diagnosis is compounded by the fact that in many cases, none of the severe initial syndromes may have presented. In fact it might be assumed that a severe, acute illness provoked a host re­sponse with complete remission, while a subacute illness did not. However, there is an overlap, and as usual it is probably too facile to be dogmatic.

Thus, for the purpose of differential diagnosis two main conditions should be considered, namely, the pathogenic agent and the organ af­fected. The host response should also be seen as a third condition that vitally affects these two factors. Considered separately in the context of the condition studied here, this can be summarized as follows.

Pathogenic Agent

Pathogenic agents may be organic or inorganic. In the present con­text most organic pathogens are viral, but, as shown later, this is not exclusive of other agents. Most of the inorganic agents are varying chemical toxins, and of these the insecticides used on farms for crops or animals, or in the home for insects on plants and occasionally for lice on children or pets, together with wood preservatives used in the home or at work, are the most common in the United Kingdom. This is not exclusive and could be extended to the ingestion of toxins on food or in water, etc. We have recorded such cases, which have caused profound paresis in some cases and in others subclinical weakness that could be classified as ME.

Organs Affected

It is obvious that either organic or inorganic toxins may have an ef­fect on varying organs and thus give rise to varying syndromes de­scribed under various titles. This depends not only on the toxin but also on the host.

Host Response

Host response is a crucial consideration relating to the previous considerations. In the case of organisms, be they virus or others, it can be shown that the host response may determine the degree as well as the site of infection. Some patients may be immune to certain or­ganisms while others may be susceptible. The degree of immunity may vary over months or years and also be suppressed by varying fac­tors (e.g., toxins), which then act as cofactors. While we are aware of this, other host factors that appear to influence organ susceptibility are not so well understood. It is interesting that antibodies may be general and circulating in serum or they may be purely local.

I showed this thirty years ago while investigating cases of infertil­ity, where sperm subjected to only one minute of contact with cervi­cal mucin died, but would survive a whole night in the female's serum. When a viral infection occurs in a family, one member may have cardiac and another CNS involvement, while the others remain free of illness. Thus a single agent may be responsible for differing syndromes. This may be explained by "local cell surface" acting anti­bodies with specific organ-protective qualities, but these antibodies also can vary over the years. Taking this into account, the differential diagnosis should not be taken to imply a different etiology. Another corollary is that identical causes, with differing syndromes, would re­spond to the same treatment. However, bearing this in mind, it is also important to see that multiorgan involvement may occur due to infec­tion; also, the involvement of one organ may have effects on other organs.

This is well demonstrated in the hypothalamic region, which has a wide supervisory role, operated via neuronal and humeral mecha­nisms. Examples of these mechanisms can be seen more centrally in pituitary regulation, with its further effects from the thyroid, adre­nals, etc. to the apparently more distant regulation of bowel motility.

These factors make an exclusive title for an illness difficult. In dia­betes there is not just pancreatic involvement, because the Kimmel-stiel-Wilson syndrome, which involves multiorgan sequelae, shows how diffuse the effects may be. Also in anterior poliomyelitis other neurological involvement takes place apart from that in the motor system. Autonomic disturbance is perhaps the most frequent, and hy­per- or hypohidrosis, systemic hypertension, and gastric hypomotility or atony with constipation, as well as sensory loss due to the posterior roots of the cord being affected, have all been recorded (Plum, 1956). In my series, cerebellar ataxia, papilloedema due to increased intra-cranial pressure, and Reye's syndrome have also occurred in the acute infective stage of viral illness, and these conditions were also reported by Curnen and colleagues (1961) and Brunberg and col­leagues. The progression from the acute to the more chronic stage in all these diseases may not follow an orderly pattern either in time or organ location, which may be diffuse, and this is reflected in the ME syndrome.

We can briefly consider some of the factors involved in virus-host in­terchange. Viruses are intracellular obligate parasites, and the host mechanism has to recognize this if it is to deal effectively with the virus. The T cell population only recognizes antigen when it is displayed on cell membranes along with a cell marker. These markers belong to the major histocompatibility group (MHC). The T cells, if thus primed to the viral antigen, recognize and bind to it and the MHC molecule and commence to produce interferons (IFNs). Anti­bodies, complement, and polymorphonuclear leukocyte deal with circulating extracellular infection, while T cells, IFNs, macrophages, and NK cells deal with intracellular infection—in this case viral. This mechanism can be thwarted by so-called antigenic shift or drift. In the first, there is movement of genomic material, while in the second, there is a swapping of genetic material from reservoirs of different viruses. This could explain the way in which one infection reactivates a latent strain.

However, both local and systemic antibodies attempt to block the rep­lication and spread of viruses, either circulating or being shed from a cell that has been infected and killed. IgG is the most prevalent anti­body of the immunoglobulin system and is a potent opsonizing agent. The complement system of serum proteins is activated by IgM and later by IgG. They opsonize target cells for the phagocytes, which are then bound by IgM or IgG, and this is the classical pathway. Cells synthesize interferon when infected by virus; it is secreted into extracellular fluid and binds to adjacent cells. Interferon-alpha is de­rived from lymphocytes and interferon-beta from fibroblasts and other cell types. The IFNs acton certain cell genes that either catalyse or retard factors responsible for protein synthesis, which in turn re­duces mRNA translation, while another factor results in the degrada­tion of host and viral mRNA. The total result is to establish a sort of cordon of uninfectable cells around the virus. Thus, viral replication is inhibited. In mice if interferon is inactivated by an antiserum, they succumb to a small viral dose. IFNs have at least three roles—to kill vi­rus, to inhibit host cell division, and to modulate the activity of NK cells.

In ME, as with certain other viral illness, T cell dysfunction occurs, and Hamblin showed an increase in suppressor activity with T cell sup­pression of in vitro synthesis by normal B cells. Also, Caligiuri (1987) found 73 percent of ME cases had a decrease in the number of NK cells, and the T3 negative subset was reduced in 50 percent. This is in­teresting in the light of the foregoing remarks, and CD4 T cells migrate from blood to tissues in virus-induced disease as viruses are intra-cellular obligate parasites. The persistent viral infection cycle is com­plex.

There may be a primary acute illness that would qualify for a defi­nition, or it may be followed by a series of other symptoms that would require further definition. In some initial infections the primary stage may not be evident, including diseases as diverse as TB and even AIDS, among many others. All of this is true of ME. Thus a search for the origin may not be helpful and the continuing multiorgan effects may be confusing. Investigations for the continuing reason for this are a challenge. In considering these problems, the differential diag­nosis of the primary illness is obviously important, and in my series some of the final diagnoses arrived at are discussed here.

• Bornholm disease, which may mimic gallstone or renal colic, torsion of bowel and pleurisy, or even myocardial infarction.

• Meningitis and encephalitis, which may be bacterial.

• Labyrinthitis is viral in most cases, but may mimic a basilar ar­tery insufficiency syndrome.

• Cerebellar syndrome may again mimic a vascular-mediated syn­drome.

• Hand-foot-and-mouth disease, with or without iritis, is usually viral, but erythema chronicum migrans (ECM) must be kept in mind as Lyme disease can closely mimic ME. Ixodes dammini, I have been told, exist in deer as near my area as Sherwood Forest. I have had one case.• G.I. syndromes, e.g., gastroenteritis and also pancreatitis, may also be bacterial, toxic, or viral. Radiculopathies also occur and may have varied etiologies, but a viral cause should always be considered.

• Flulike illnesses may have varied and obscure causes. Serological titers often are not performed, although it may well be wise to do so for future reference, in case chronic sequelae occur.

Chronic Sequelae

The more challenging task involves chronic sequelae, which is particularly true in ME as the effects may be neurological, hormonal, autoimmune, or myalgic in varying degrees, and the latter may in­volve the myocardium. All of these may be discrete but also may oc­cur as an additive in ME, which of course tends to cause problems. Moreover, the difficulty lies in the fact that the pathogenesis of the acute stage might not have been accurately defined. Because of my interest, serological titers were usually performed on more than one occasion in those presenting with a well-defined illness as shown in the previous list, but some patients with a flulike illness did not pres­ent until secondary effects developed. In these, the definitive liters may have fallen and culture was often negative, but the VP1 test de­veloped by Professor Mowbray has proved of considerable value for suggesting ongoing enteroviral infection.

Conditions considered in this work, which again are not exclusive:

Brucellosis—This may be difficult to define, and only one was proven in this series. However, it can produce all the acute and chronic symptoms alluded to in this work. In the CNS, diverse spinal and cerebral syndromes occur, sometimes with paranoid delusions. Endocarditis may cause emboli with remote effects.

As with toxins, this should be considered in those who work with animals. However, the ESR is high, and lesions may de­velop that mimic sarcoidosis. The ELISA IgM in the acute stage or IgG in the chronic stage should be assayed. Lyme disease—As with brucellosis, it is difficult to prove in the chronic stage, and I have only seen one, which was considered but never proven. Lyme disease causes ECM skin lesions in the acute stage, which may be confused with hand-foot-and-mouth (HFM) disease. In the later stage neurological, cardiac, and arthritic condi­tions may follow, as with viruses. Lyme disease, however, is due to a spirochete transmitted by ixodid ticks.Tuberculosis—One was referred as ME but had a very high ESR, which is most unusual in ME. TB may have an obscure location, as was the case here, which was eventually shown to be renal. Carcinomas—Again, they usually have a high ESR. This is dealt with in another context in Chapter 8 and may be primary or se­quential.Endocrine—This is dealt with in Chapter 5, but thyroid antibod­ies as well as diabetes can develop in these patients and be a complication in the ME syndrome.

CVS—Pericarditis, perimyocarditis, and myocarditis have all been noted in this series as discrete or additive. The additive cases still manifest the symptoms of ME after the cardiac condition resolves. CNS—A list of other syndromes that have followed well-docu­mented viral illness has been listed, but most, in my experience, can be excluded by careful examination, using MRI scans, etc.

Auto-immune—This is a difficult area, and autoimmune sequelae are well recognized following viral infection. However, they should be differentiated clinically as a separate entity or as an additive factor in ME.

Toxins—A small number have been seen and serologically proven. They can give rise to serious illness and should be borne in mind. They do have a depressive effect on bone marrow, which also occurs with viral infections. Jacobson and colleagues published the results of a good study in 1987. In these cases the serum folate was low, below 3 ug/L, which is the lower limit of normal. They reported that in half to three-quarters of all such patients, an unexpectedly low serum folate was found. In twenty-nine patients it was as low as 1.6 ug/L. Patients with nor­mal values had on average 5.8 ug/L. Folate is required for hemopoiesis and for the conversion of uridylate to thymidylate of DNA and for all other cells and tissues. It is necessary for the synthesis of purine rings and of RNA and proteins. All infection causes a bimodal response of the immune system in cellular multiplication and synthesis of immunoglobulins, both of which are folate dependent. Repair in pulmonary and skin lesions makes demands on folates also.

A high incidence of folate deficiency was found in those who had viral skin rashes. Also, Behan and colleagues (1985) noted this folate lack in cases of ME. However, thirty or more years ago I noted the association between folate levels and fetal abnor­mality, particularly in tissues deriving from ectoderm. Not infre­quently, this was also linked with a viral infection at or just before the time of conception. It is also relevant that insecticides have been incriminated in fetal abnormality. The question then arises as to whether virus or toxin lowers the folate to danger lev­els, or whether a low folate level allows the body to be suscepti­ble to infection. I suspect the former, but it still begs the question—Is it the virus or the low folate that actually mediates the neonatal pathology or adult illness?

The question is sometimes asked, "Do women with ME have an in­creased risk of bearing children with an abnormality?" The simplistic answer is "No." However, I did a study in a group of women of child-bearing age (seventeen to thirty-seven years) who had a viral illness with at least an eightfold rise in Coxsackievirus titer and had become pregnant or had developed the illness during the last trimester. In that study, 68.2 percent had normal children, but there was a rather high number, 31.8 percent, which were abnormal.

Broken down, the abnor­mal cases included: two aborted (3.0 percent); six stillbirths (9.1 per­cent); eleven fetal abnormalities (16.7 percent); and two babies who died from cardiac complications (3.0 percent). However, I emphasize that this is not related to ME but does relate to the pathogenicity of the enteroviral group of viruses.

The important consideration, however, is that the syndromes out­lined may all cause chronic illness, and some may actually coexist with ME and have the same etiology, while others may mimic the condition. A very careful history written by the patient, which both saves time and is much more reliable than question and answer (which may be bi­ased), should, in most cases, define the issue. The exercise can alert us to the possibility of occult infection in conditions that may cause chronic malaise. The persistence of spirochetes and viruses should by now be well recognized, but the investigatory proceedings needed in some cases, in my opinion, require more intensive laboratory investiga­tions.

It may be helpful to review the "response to stress" and see the inter­play of neurological and hormonal activity, which can be seen as an "efferent" response by the host. By the same token, there is an "affer­ent" result from the response of the immune system. This integrated function determines the whole pathological scenario, felt by the patient and perhaps perceived by the medical investigator, but this depends upon signs, which are often less obvious than symptoms.

I had the rare pleasure of interviewing Dr. Judy Mikovits at the IACFS/ME conference in San Francisco last March. Dr. Mikovits is best known for her involvement with XMRV research.

Dr. Mikovits is a cellular and molecular biologist with over 30 years of scientific expertise. She has directed programs on HIV, cancer, epigenetics, and neuroimmune disease, with a focus on development of novel drug and diagnostic technologies. Dr. Mikovits holds a PhD in Biochemistry and Molecular Biology from George Washington University. Her dissertation was on HIV latency and mechanisms of immune activation in monocytes. Dr. Mikovits was a Postdoctoral Scholar in Molecular Virology at the Laboratory of Genomic Diversity, National Cancer Institute under Dr. David Derse. Over the past 26 years, she has published 51 scientific papers in peer-reviewed journals.

The riveting story of XMRV, and the subsequent scandal which left her career in ruins, is told in Dr. Mikovits' forthcoming book, Plague: One Scientist’s Intrepid Search for the Truth about Human Retroviruses and Chronic Fatigue Syndrome, Autism, and Other Diseases. It was a journey that took Dr. Mikovits through the process of scientific research, the thrill of discovery, and ultimately to the high-level corruption which eventually led to her arrest, and the conviction and sentencing to federal prison of her employer, Harvey Whittemore, for federal crimes that, in the words of Nevada's highest court, reflected badly on his “honesty, trustworthiness or fitness as a lawyer.”

In spite of the notoriety surrounding XMRV, Dr. Mikovits remains committed to helping people who suffer from ME/CFS and is determined to discover its cause. “To me,” she says, “it's the patients that matter.”

Dr. Mikovits continues to work on neuroimmune disease and cancer at MAR consulting, an endeavor she shares with Dr. Francis W. Ruscetti. http://www.marconsultinginc.com/home.html

Plague will be released on July 1. You can pre-order it now from Amazon at a guaranteed 30% discount. (Note: This discount will not be available after the release date.) Order here.

That's a good story. In late November of 2005, I met Kristin Loomis, the head of the HHV6 Foundation. Kristin visited my lab and got excited. Her daughter, who was very sick, had been diagnosed with CFS, but Kristin thought she had HHV6. What I saw in Kristin Loomis' daughter was an astounding loss of intelligence and cognitive function, which was striking in such a young person.

At the time, my company, EpiGenX Pharmaceuticals, was being sold, and I didn't have much to do. So, I agreed to work for Kristin as a consultant on HHV6, to put the research together. In 2006, Kristin sent me to the HHV6 meeting in Barcelona where I met Dan Peterson. He gave a very compelling talk. His data showed clonal rearrangement of gamma delta T cells; you don't get clonalities like that unless you've got a frank cancer. He said, “I don't see where all this cancer is coming from. I don't know what it means. If anybody can help me, see me after the talk.” I took one look at the slide, and I could not get to him fast enough. He invited me to Reno, where I met the Whittemores.

So, you got hooked because you saw something very strange.

It was the mantle cell lymphoma that was the red flag. Dan Peterson had five patients with mantle cell leukemia in a group of 100, which appeared to be a cluster. The way I've been trained, I look at cancers and I look at clusters. So, I thought, “There's something going on,” because mantle cell lymphoma is incredibly rare.

Did you know anything about ME/CFS before you met Dr. Peterson?

At that time, CFS was really nothing to me, because when I looked at the literature I thought, “Fine, they've got an NK problem.” That makes sense, because NK [natural killer] cells only do two things, they recognize viruses and they recognize tumor cells. So, if you can't clear viruses, you're going to have NK cell disturbances. After I met Dan, I purposely didn't read the research, because I wanted to discover what was going on without being influenced by previous research.

The one exception I made was a paper by Paul Levine. His paper was about families that had children who had cancer and CFS. NK function was lowest in the children with cancer. But CFS patients had only slightly more NK function. I carried that paper in my backpack wondering why.

How did you begin working with him?

To me, it's the patients that matter. I basically saw a sick patient population – and they were so sick. These were young people, the promise of the country. Something had to account for it.

From the day I went into the field, I saw a crippled immune system. That's what Dan Peterson showed me – a crippled immune system.

So, all that summer I worked with Dan Peterson. We took multiple samples of the most severely ill patients. We took samples every six weeks, so we developed a very good database. It's important to have a database like the one we were creating, because if you do a snapshot of an immune profile, you capture only one day. You might miss something. The virus(es) may be latent, so you have to take repeated samples over several time points, months apart.

That was how we found XMRV. We didn't see it in of 67/101 samples, we saw it in 67/101 patients. And we had multiple samples from every patient taken over a two-year period. The reason we needed so many samples was that there could be DNA silencing of the virus by methylation, the very mechanism that was the basis of my startup, EpiGenX.

For me it made perfect sense based on my decades-long work on HIV and HTLV-1. I had published a paper on how methylation of immune modulators in HIV-infected people silenced the virus, and now I was finding something similar with CFS. [DNA methylation suppresses the expression of endogenous retroviral genes. It plays a crucial role in the development of nearly all cancers.]

Do you still believe a retrovirus causes ME/CFS?

We never said cause. It was the adversaries that said cause. What we said was that there was an association. Everyone wanted to make this virus like HIV, but it's not like HIV. It's not crippling the immune system so badly that people are dying quickly. And it's not a large visible cell component that is being crippled, like the CD4 T cell.

If you want to find a retrovirus you've got to grow it in a dividing cell, because it needs cellular genes to multiply, and it's not easy to find. So we used the classic techniques. And the association with XMRV was very strong. We had a transmissible retrovirus from the third family of retroviruses. It was first associated with a cancer, and now we found it was associated with a neurological disease, just like HTLV-1.

If XMRV was a lab artifact, why wasn't it in all the samples – those from healthy people as well as from those who were sick?

Only the samples we sent to Silverman's lab got contaminated, but these were all samples from patients. So samples from healthy controls didn't get contaminated.

In our paper, the hypothesis was that we would find a retrovirus. We did experiments in 2008 that did not quite match Silverman's XMRV plasmid sequence. Because we couldn't make the match with Silverman's XMRV, we modified the parameters. We changed the PCR reaction to capture everything that wasn't an exact match. This is what we call “wobble” or “variation.” Max Post was the person who captured the variation in our samples.

When we pulled those pieces out and sequenced them, we were getting similar, but not exact matches with Silverman's XMRV.

Silverman asked for 30 samples, which we provided. But he wouldn't do his work blinded, so he knew they were from patients. Our work was blinded, but my notebooks were the only way you could figure out which sample was associated with which patient. Silverman provided his own controls.

So, after three tries Silverman still couldn't get a full-length sequence of the virus we were looking at. That meant that what we sent him simply was not XMRV Silverman. He said in March 2009, “Let me try again.” We replied, “No, there's too big a chance of contamination.” But Lombardi cultured the virus and sent Silverman the samples anyhow without telling me. That was a mistake. When Silverman sequenced those samples – which were not blinded – in his laboratory, they got contaminated. Silverman had lots of plasmid in his laboratory, as he had been doing all the sequencing. He notified us in July of 2011 that our samples were contaminated with his VP62 plasmid.

But even if what we found wasn't Silverman XMRV, it was still associated with two diseases – the lymphoma in Dan’s patients and CFS. It could have been a family of viruses, or a different strain. For example, there are five strains of HTLV, and only one is pathogenic. What we found could have been just one in a family of retroviruses.

A good example of this problem is Dr. Lipkin’s research. Dr Lipkin says he has found evidence of retroviruses in Montoya’s samples of ME/CFS patients, but he claims this probably doesn’t mean anything because he also found them in the controls. But what if the controls have a non-pathogenic strain? No one has a detailed sequence that would enable anyone to know those answers. And only 5% of the people infected with HTLV-1 ever get disease.

After 40 years we still don’t know the exact mechanisms of how HTLV-1 or HIV cause disease and why the other very closely related strains do not. The point is that healthy people do not express human retroviruses endogenous or otherwise! Of course there are missing links, but to abandon a line of research that could help millions of people is just bad science.

So, if it wasn't Silverman's XMRV plasmid, what virus did you find in Dan Peterson's patients?

We isolated a gammaretrovirus from at least one person. And I believe beyond a shadow of a doubt that it was a new gammaretrovirus that could infect humans. The way we found it was by using a reagent called a 7C10 monoclonal antibody, which was an antibody to murine gammaretroviruses. That antibody recognizes all known murine gammaretroviruses.

The problem was that every time we put our sequence in the database it came up with XMRV, because that's all there was. There was nothing else to compare it to. When De Freitas did her work in 1990 she had the same problem. She found HTLV-1 and HTLV-2-like virus because, back then, that's all there was in the database.

So, every time we put a sequence in the database, it came up with XMRV because there was nothing else to check it against. But you have to remember that XMRV isn't a single virus, it's a family of viruses. And there may be many other retroviruses that are similar to it that may be pathogenic to humans. We just don't have a way of identifying them through a database right now.

If you found a new retrovirus, why was the paper you published in Science retracted?

The paper should not have been fully retracted. It should have been partially retracted. The only reason the paper was fully retracted was because I was jailed and had no access to our data.

One of the things that was so wrong about what happened is that they threw out all my research. They destroyed it all. And this is the saddest part; we came up with a study that showed who would do well on Ampligen. 30% of the people with ME/CFS had antibodies to spleen focus-forming virus (SFFV), and these were the patients who responded to Ampligen.

What we had found was a biomarker - the antibody to SFFV-env recognized by 7C10. This finding was later validated in the Lipkin multicenter study. The assay in our original paper was replicated in every study we did, but now all of that original data is lost. If I hadn't been so thoroughly discredited, and my research destroyed, Ampligen could have been approved.

But I look at it this way, if that Science paper on XMRV had never come out, would we have the research that is being done today?

Why did you call your book Plague?

One of the reasons we called it Plague was not so much because of the disease itself, but because of the increasing numbers we are seeing of people developing related health problems, such as autism, neuroimmune disease, and cancer. If we do nothing, in another decade one in two families will have one of these neuroimmune diseases.

From another standpoint, the title refers to the plague in science. There is a plague in medical research. We don't want to believe that medical research is corrupt. We don't want to think that if they saw a child who was sick, researchers wouldn't do something. But yet, the government is corrupting science – just as they did with ME/CFS and XMRV – by controlling the funding and the message, which ultimately determines what the journals publish.

What have we learned?

That is the question I ask myself.

XMRV was made in recombination with mouse cells. Before we could grow cells in labs we would pass cells through mice in order to attenuate them. But we found that by passing cancer cells through mice we could grow tumors; the cells had recombined with a retrovirus. Everyone before 1980 did this. It was standard laboratory procedure. We learned that anything we passed through animal tissues could make replication competent recombinant retroviruses in only ten days. All of our NIH research is based on mouse research. And those cell lines I worked with daily for more than 30 years have the potential to produce novel retroviruses.

So, here's the question: How many of these recombinant retroviruses are now in our environment and playing a role in all of these neuroimmune diseases?

If XMRV had mutated only two amino acids in its genetic envelope we could have had a true plague. Nobody could have predicted that XMRV could remain stable on a bench for months, or that it could be aerosolized and transmitted in dust, in saliva. But because our immune systems spotted it, we developed an antibody. (Many of the lab workers such as Max and myself seroconverted, meaning we developed the antibody from our lab exposure.)

How many people did we save by learning that XMRV could be aerosolized and spread to immune-compromised individuals or lab workers? We may have avoided something that could have infected everyone, because Silverman was sending XMRV all over the world.

But. exposing Silverman's XMRV as a lab artifact should not have ended the research. The work Frank Ruscetti and I did to find the epitope that the antibody recognizes in humans should have been completed. Currently 6% of the population carries an antibody that recognizes a gammaretrovirus envelope protein. Six percent is 20 million Americans!

Last year, Gary Owens published a research paper that showed the envelope protein of MLVs alone could cause vascular leak and aggressive tumors. He had previously published data identifying XMRV-2, now called B4RV, on November 10, 2009. That was only one month after our paper was published. We worked with Gary and found those sequences and proteins in some of our original patient samples. The virus Gary Owens found causes the very things I saw in Dan Peterson's patients and which are found in so many of the complex chronic diseases that affect our population today. So why was this work suppressed for three years, and why is it being downplayed now? How many new retroviruses have we created through all the mouse research, the vaccine research, gene therapy research? More importantly, how many new diseases have we created?

When they destroyed all of our work, and discredited everything I or Frank Ruscetti had ever published, and arranged for the publication of my mug shot in Science, the NIH very deliberately sent the message to researchers everywhere about what would happen to any honest scientist who dared ask those important questions.

If HHS gave you the power to re-name CFS, what would you call it?

Non-HIV AIDS. It is an acquired immune deficiency, beyond a shadow of a doubt.

The following interview with Sonya Marshall-Gradisnik appeared in Get It Magazine. Marshall-Gradisnik's contributions to the field of ME/CFS research have been impressive. Here she talks about how she got involved in ME/CFS research, and offers some insights into her work.____________________

Professor Sonya Marshall-Gradisnik from Griffith University is a biomedical researcher specialising in Chronic Fatigue Syndrome.

She and her team are leading the way in extraordinary international initiatives being fostered right here on the Gold Coast.

"You're one of the world's Ieading biomedical researchers specialising in Chronic Fatigue Syndrome (CFS). Can you explain some of your most exciting recent findings and what they mean for sufferers of CFS?"

The CFS research team that I lead has found significant changes in white blood cells in CFS patients. White blood cells are important as they are the cells in the blood that fight off infections, viruses and bacteria. We have found the function of these cells has been significantly reduced and we have also found significant changes in some genes that control the function of these white blood cells. Collectively these findings suggest these white blood cells may be involved in the pathology of this illness. Furthermore, it gives us hope that we may be able to identify CFS patients using these changes as currently there is no diagnostic test for CFS. Consequently diagnosis of CFS takes typically greater than twelve months which can be not only frustrating for the patients as they do not have a timely answer, but it is very costly to the healthcare system as a number of unrelated tests have to be conducted to ensure the patient is negative for these other tests prior to being confirmed with CFS.

"You've managed to secure several million dollars worth of competitive research grants. How difficult is this process, and how important it is to continue this research?"

It is extremely difficult to secure research funding for any type of biomedical research and applying for funding CFS biomedical research is I think even more difficult due to such factors of the stigma associated with this illness. However, in saying that, the Queensland government and the Mason Foundation, which is a national funding granting agency, have significantly provided me with research funds where the findings have been world first and suggest the possible involvement of the immune system in the pathology of this illness. I am very of proud these findings and the world first results we continue to report, as they are unravelling the potential cause of this illness as well as they show we may be coming up with some markers that may assist in early diagnosis of this illness. The development of a screening test using these potential markers we have found is an area that we are developing, as this test could be applied early in a patient's illness which may not only help the patient and the physician, but also help reduce healthcare costs.

There still is a great deal of research to be undertaken in this area as my team as well as other groups at Stanford University are now focusing on genes and how cells communicate. We are only beginning to understand the possible role of the immune and the endocrine systems and potentially how they may be involved in the development of CFS, so this area of focus in CFS remains a high priority for our team and international groups as well. There is still so much to be done not only in the research area but also in helping CFS patients with a clinic that has physicians where CFS patients can visit to work with their regular doctor to assist them with their illness. Finally, as CFS symptoms vary - some CFS patients are profoundly affected with not only being fatigued, but they are predominately affected with significant changes in memory function, cognition, cardiovascular and gastrointestinal health problems; these collective clinical symptoms and the severity of these symptoms need further investigations.

"You've established the first Australian CFS research/medical clinic at Griffith University; what will it mean for people to now have access to such a facility?"

There has been significant interest locally, interstate and overseas from CFS patients and clinicians. This clinic is located in the Griffith Health Centre, where our research centre is also located. Having the clinic and the research centre in the same building will enable patients to have access to clinical services as well as potentially participate in CFS research we are conducting. This model is truly unique as it is the only research and clinical services to be offered anywhere in the world to be housed under the same building which is unique and has not gone unnoticed by international agencies, such as the Centre for Disease Control and Prevention (USA) and members of the Medical Research Councils (UK) who visited in December last year.

"How did you originally become interested in this area of research?"

I am an immunologist and back in 2007 I met an amazing clinician from Queensland Health who was, and incidentally still is, as passionate about biomedical research in the area of CFS. Back then we both had a few ideas and tested them in a couple of small CFS research projects with one research student. Let us say the results were promising and it snowballed from there.

"What is your advice for young women aspiring to work in a science based career?"

There is no substitute for hard work; however, it is also important to surround yourself with positive people who also share your vision and are able to offer you guidance as well as keep you on track. It is always important to seek advice and listen to those around you as no one ever knows all the answers. These are key areas that I think anyone who would like a career in science may need to follow in the first instance, and then as your career develops establishing a network of people not only in science but outside your field to ask advice enables you to assess everything from different angles which is often invaluable. Always stay in contact with your peers as this is an invaluable network that will enable to you to tap into people that may have other resources and skills that you may need and it enables you to develop/complement your skill set as you progress throughout your career.

I will not deny, a career in science is hard work and the hours are sometimes challenging. However, to develop a question that you can test and see if it is correct (or not) is truly wonderful as you are able to work like a detective and also think creatively - I have the best job!

"What are your goals for the coming couple of years?"

For the coming twelve months I have some big objectives as I would like to set up the first Australian Brain and Tissue bank for CFS patients. This will enable research to progress very rapidly as researchers would have access to tissue to assess potential changes in these tissues and how this may be key in the development of the illness. This ultimately may lead to clinical trials in the coming years.

As CFS has varying severities, some CFS patients are isolated at home as they are house bound or\ bed bound and vary rarely are able to have consistent medical attention. These patients mostly communicate through social media and it is for this reason I would like to achieve in the coming twelve months to fund raise for a mobile patient transport vehicle. This will enable patients to be collected from their homes and be transported to the CFS clinic or if they have other medical appointment as currently there is not such services available in Australia. I would like to raise the funds for such vehicles where patients in the south east Queensland area or Northern NSW region would have access to the CFS clinic and allied health services.The ongoing research that I lead I would hope grows from the current group of 10 to be larger, and is even more diverse in the area of developing a nursing model of care for CFS patients.

Currently I am liaising with a national pathology collector to assist me with allowing me to have pathology collection sites in Sydney,Melbourne and Canberra for CFS patients so they are able to have their blood and tissue collected, where these specimens are transported toour research centre to further examine the possible role of the immune, genes and endocrine systems in the possible role of this illness. In turn, further enhancing the CFS research and clinical database that has been developed by the national research centre I lead.

Sometimes the objectives I set may seem overwhelming, however, the challenges CFS patients face are far more significant, and for that reason I think my objectives are not too great.

First published on ProHealth as Noted Activist Tom Hennessy Passes Away After 25-Year Battle With MEOn Monday, September 9, 2013, Thomas Michael Hennessy, Jr. passed away in Boca Raton, Florida after a 25-year battle with ME/CFS. He was 59 years old. The family will receive friends at Our Lady of Mercy Catholic Church, 9200 Kentsdale Rd., Potomac, MD on Thursday, September 19, 2013 from 10-11 AM with Mass of Christian Burial following at 11 AM at Interment Gate of Heaven Cemetery. (You can read the obituary here.)Tom Hennessy's contributions to the ME/CFS community have been enormous. He was the originator of International ME Awareness Day on May 12th, and founded the advocacy organization RESCIND (no longer online). Although he was severely ill, Tom testified eloquently, and passionately, at numerous national and international ME/CFS conferences and meetings, never failing to drive home the point that people with ME aren't tired, but sick.Before falling ill with ME in 1988, Tom was a successful sales and advertising executive in Marin County, California. In spite of what he described as “chronic mono” following a severe flu, Tom continued to work 12-hour days, until a final collapse left him bedridden for 18 months. He never recovered.On April 15, 1989, Tom was asked, at the last minute, to speak at the first international CFS conference, held in San Francisco, California. In his own words, Tom gave an “in your face” speech, which stole the show. “We are SICK, often deathly ill, and we are NOT fatigued!” he said. “If you do NOTHING else today, then lock the doors, get together and knock heads and come up with an ACCURATE definition and CHANGE THE GOD DAMN NAME!”

This speech catapulted Tom into the national spotlight, and from that day forward he remained a fierce advocate for legitimizing the illness in the face of government and insurance industry attempts to minimize the devastating effects on individuals who contract ME/CFS, as well as its cost to society as a whole.No one could have stated the case for the eradication of the demeaning name "chronic fatigue syndrome” better than Tom himself, so I am including the full text of his 2011 CFSAC testimony below. His words deserve to be read, and re-read, many times over. In the wake of worldwide efforts to classify ME/CFS as a psychiatric illness, and of the virtual incarceration of Karina Hansen, on the heels of the recent attempt by HHS to redefine ME/CFS out of existence, in the CDC's continuing failure to adopt an accurate case definition, in the NIH's refusal to fund research, in the black-listing of medical professionals who seek to treat patients with ME/CFS, and in the subversion of the very agencies and organizations that are supposed to represent our interests, but instead seek to undermine us, Tom's words still ring out loud and true.

"There are NO more excuses. Slow people need to learn by repetition, so I again say, the theme for now and the future is 'NO MAS!' [No More!]"(Note: You can read Cort Johnson's excellent interview with Tom Hennessy here.)_________________________________________Testimony Thomas Hennessy, Jr.Good Afternoon Chairman Snell, Dr. Wanda Jones, members of the M.E.AC committee, Ladies and Germs, as Charles Dickens once said, "These are the best of times. These are the worst of times..."I want to PUBLICLY thank Dr. Wanda Jones and entire M.E. Accountability Committee staff for scheduling this meeting on the 10th and 11th of May, so that advocates can both testify to this committee AND try to meet with their respective senators and congressmen on May 12th, the 19th anniversary of ME/CFS/GWS/FMS/MCSS and Chronic Lyme disease Awareness Day. Also, after more than 2 decades of requests from the patient community, HHS has finally made this meeting available on the Internet, so that the millions of sick people around the world can have access to these meetings. I thank you ALL on their behalf.

A lot has changed in the past six months. But, a LOT more needs to be changed. There IS enough research money. it is just going to the wrong places. [Here Tom requests a slide of NIH Categorical Spending.]

Thanks To Dennis Mangan, Dr. Vivian Penn, Dr. Wanda Jones, Chairman Christopher Snell, NIH Director, Dr. Francis Collins, and HHS Director Kathleen Sebelius and all the folks who participated in the very informative "State of the Knowledge" workshop held at the NIH in April, all the key players now know that we are NOT a bunch of meretricious valetudinarians. We are very sick and in chronic PAIN!! The time for being treated as a piece of dog feces under the shoe of our medical officials and government bureaucrats, and dishonest insurance executives is OVER! NO MAS!The late, great Eleanor Roosevelt once said, "You can NEVER be a second class citizen without your consent!" AMEN. The time to be referred to as being "chronically fatigued" is OVER! NO MAS!

If patients en masse REFUSE to accept the label "CFS" anymore, and the doctors refuse to DIAGNOSE UNDER THIS ASININE LABEL, IT WILL DIE ON THE VINE! Myalgic Encephalomyelitis has had a valid WHO code as a neurological illness for 40 years! USE IT! There are NO more excuses. Slow people need to learn by repetition, so I again say, the theme for now and the future is "NO MAS!"Dr. David Bell once referred to this as "the disease of a thousand names". I say the exact opposite. This is 1,000 disease entities under ONE name! Louis Pasteur said more than 100 years ago, "The antigen is nothing, the terrain is everything!"

As I said in my first speech to the very first International "CFS" meeting in 1989, "We are NOT sick of being tired, We are tired of being SICK!" There is a HUGE difference!! Webster's Dictionary says 'to define is to make clear and distinct, to differentiate.' If you do NOTHING else today, lock the doors and come up with an accurate definition and change the God Damn Name! If you do not have the courage to do this today, you will condemn untold millions of people from all over the world to lives of abject misery, premature deaths and a huge economic burden on our societies. Knock heads until you come up with an accurate definition and a proper name."

That Date was April 15th, 1989. the day before my 35th birthday. Despite seeing some of the top doctors in the world, and trying more than 100 different medications, supplements, meditations, prayer groups and more, I still have not been able to work ONE single 8-hour day in the past 23 years! The good news is that we have a good definition, we need to adopt the Canadian Consensus Definition, by Carruthers et al TODAY and scrap every other definition in use anywhere in the world. Period! Go with the name Myalgic Encephalomyelitis, which is not a perfect name, but it describes a CIND (Chronic Immunological and Neurological Disease) which has had a WHO classification for 40 years. The Canadian Consensus Definition must be adopted worldwide immediately. all other definitions and names need to become moot. Immediately. (Sign the petition here.)

The CDC "CFS" website must be taken down and rewritten immediately! The entire staff of the CDC "Viral exanthems" division from Dr. William Reeves and Dr. Elizabeth Unger, Jim Jones et al need to fired immediately and given NO severance whatsoever. Their so called "work product" for the past quarter of a century has been abysmal. What they claimed to be affecting some 4,000 to 10,000 Americans in 1988, they NOW claim affects 1 million to 4 million people! If AIDS, Heart Disease or Cancers went from 4,000 people to 4,000,000 people in 25 years and you worked for the "centers for disease control" in corporate America, they ALL would be fired! No severance, no mercy, NO MAS!

I have read 25,000 letters from all over the world. Hard working, ethical young men and women contract some type of Agent "X", which causes dysfunction of the autonomic nervous system. Many ignorant and arrogant psychiatrists, most from the damn 'Simon the weasel' school in the UK have pushed GET and CBT theories to cure VERY PHYSICALLY SICK PEOPLE by forcing them to exercise their way out of being SICK. This is a crime against humanity! We are for the most part, HARD WORKING, ethical, often even athletic people who have pushed ourselves too hard already. We are NOT deconditioned because we are lazy or fearful of exercise. We are SICK!

I have tried to push Chairman Christopher Snell behind the scenes to film EVERY patient that goes through their "Stevens Protocol." Insurance companies like UNUM Provident will continue to use outdated, dishonest criteria that they bribed weasels like Simon Weaselly to "delay, deny, and hope you die!" as long as we let them. They are out to collect premiums, and then "delay, deny, and hope you die" when sick people make legitimate claims.

Chairman Snell tells me these same patients almost always WIN their disability cases when they reach the Administrative Law Judge stage, which is often 2 to 3 years after filing their disability application. And since 40% of all Americans have net worths less than $2,000 this is a calamity which will only get worse! I believe that most patients will gladly give permission to allow themselves to be filmed which will PROVE that we can NOT do any "sustained physical or mental effort for one, two or three days in a row." This group of conditions is caught between the Autism spectrum disorders in young, immature nervous systems, and Alzheimer's on the other end of the spectrum.

This is an international calamity that will bankrupt the Long Term Disability industry, so they have and they will continue to lie, cheat and steal premiums and then write in the small print in their contracts that if you are diagnosed with "CFS" or "FMS" you only get two years lifetime disability payments. Then they give "VULTURE awards" for the claims adjusters that deny the most "CFS" and "FMS" claims. They all should be given Rodney King style beatings every day of their lives until they "get it."

We are no longer going to be the doormat of the medical industrial complex. We suffer from complex, devastating Neuroimmune diseases. The joke in our community is that knowledgeable doctors who encounter new M.E. patients in their practice say, "I have good news and bad news for you..." When the patient asks, "What does that mean?" the M.E. literate doctor says, "The "good news is that this disease probably won't kill you ... and the bad news is that it probably won't kill you."

Dr. Nancy Klimas, who has treated AIDS, GWS, and M.E. patients, said if she had to contract HIV and AIDS or M.E. in today's world, she would choose to contract HIV! Dr. Marc Loveless, who also treated more than 2500 patients with both diseases, stated under oath in front of the U.S. Congress that his "M.E. and CFS patients are more sick every single day, all day, than his AIDS patients are just two months before they die!" We are like dying Hospice patients every day of our lives and we have been treated as criminals and vagrants. This must end RIGHT NOW! Again, I say "NO MAS!"

I have heard strong, brave people give similar stories of abject misery to this committee and its forerunners for two and one half decades and they have all fallen on deaf ears until the now infamous WPI SCIENCE paper of October 8th, 2009! Some group has to go to the WPI and repay the Whittemore family EVERY single dime they have invested in their WP Institute, for no other reason, than getting the HHS director Sebelius, NIH Director Dr. Francis Collins, and even President Obama to utter the words "CFS" and "serious, devastating, extremely debilitating" in the same sentence. So, there are NO more excuses for delaying, denying and hoping that we will wither away and die, using ignorance as an answer...NO MAS!I have heard patients who have lost their marriages, their careers, their families, their friends and far too often their very lives to the disease compare it to a life sentence in solitary confinement, without parole. All the while being tortured every single day of their lives. NO MAS

In 1989, I estimated annual GDP loss to the U.S. economy alone was more than $9 billion! Now, Lenny Jason and others estimate that the losses are somewhere between $18 million and $23 billion. So, our medical establishment is not only cruel, they are STUPIDNext, Medical Education! Many of the good doctors who have treated us are nearing retirement. With virtually NO curriculum regarding M.E. at major medical schools, this is a disaster that is going from very bad to a true crisis. We need to pay EACH clinician like Dr. Susan Levine, Dr. David Bell, Dr. Paul Cheney, Dr. Nancy Klimas, Dr. Chuck Lapp, Dr. Dan Peterson et al, who have treated at least 1,000 M.E. patients in a clinical setting. Each of them should be given a stipend of $250,000 and given ONE year to rewrite the CDC website and come up with pamphlets that give the Canadian Consensus Definition, and the most effective tests that need to be done, and the most efficacious treatments available. The CDC and NIH need a 24-hour a day hotline that is staffed with knowledgeable people who can answer questions for people who are too poor and too sick to travel to the acknowledged experts

Public Education! Patients who are doing their best to cope under impossible circumstances are subjected to verbal and physical abuse by people who have been persuaded by the powers that be that patients are either lazy or crazy and can be cured by thinking happy thoughts and rising Lazarus-like from their beds. “Just go back to work!, GET and CBT will cure you.” It's absolutely criminal... NO MAS!

Some 90% of us have one or more documented sleep disorders. When the body cannot get to deep restorative sleep, it cannot repair itself, which disrupts the autonomic nervous system even further. Sleep disorders need to be diagnosed and treated by any and all means necessary,

We need DRAMATIC INCREASES IN FUNDING! Not one penny less than $250 million per year, until we catch up with other serious illnesses. Anthrax research has gotten close to a BILLION dollars in NIH research money since 9/11 and yet the "CFS" budget has decreased. Maybe six to 10 people have been injured by Anthrax...and yet, Anthrax has gotten close to a billion dollars in the past decade! Pat Fero's excellent presentation at the State of the Knowledge workshop meticulously dissected the misallocation of taxpayer funds at the NIH over the past 25 years. [Videos of her presentation can be viewed here and here.] The funding for M.E. is NOTHING at the NIH. and the dismal funding for the "CFS" crap is less than 1/10 of 1 percent of the annual cost to the economy of having us lying in agony in our beds and contributing nothing to society. If you can get us back to work, we will make that back in income taxes in under a month!

The Centers of Excellence have been defunded. We need to RE-FUND them. The WPI must be reimbursed for every dime that the Whittemore family has INVESTED to help find the causes and treatments for Neuro-Immune Diseases.When I asked fellow patients if they wanted me to make any specific comments to you six months ago, the biggest response I got was “Why bother?”This group has made leaps and bounds improvement in the past six months. Keep it up! So, In conclusion I say to you NO MAS!!!

Adopt the Canadian Consensus Definition TODAY! Discontinue every other "Definition" on the planet. Declare them null and void.

Join the almost 10,000 names on the M.E. Definition that has a link at our Rescindinc.org website. if you have not signed yet, do, so. When we hit 10,000, we are taking the signed petition to the White House in a giant wheelbarrow.

Demand NIH funding of not one penny less than $250 million for fiscal year 2012. Take the money from the ANTHRAX budget. That is just slush fund for the Pentagon anyway, and Anthrax has sickened less than a dozen people since 9/11. We have close to 1,000,000 homebound or bedbound people suffering from the WHO neurological and immunological disease of Myalgic Encephalomyelitis.

Get clinicians and researchers who have seen at least 1,000 patients in a clinical setting and give the top ten a stipend of $250,000 to completely rewrite the CDC website and decide WHERE and how to spend the $250 million coming out of the Anthrax budget at the NIH.

Reimburse the WPI for every penny spent so far by the Whittemore family, and fund trials, PROPER replication trials, for XMRV and the National CFIDS Association of Gail Kansky's ciguatera isotope found by Dr. Hokama, one of the top marine biologists in the world. Virtually every serious M.E. patient they have tested has been positive.

Fast Track Ampligen. Look at Mary Schweitzer and Bob Miller. They are living proof that this drug can help people. Dr. Carter and company are poor managers. I say that the Pentagon should declare this disease group a national emergency and they should nationalize HEM and give Dr. Carter a royalty for every treatment of Ampligen, and use the Pentagon funding to do trials on sick Gulf War veterans and any patients who want to enroll.

Refund the Centers of Excellence for Dr. Jose Montoya at Stanford, and Dr. Klimas in Miami, Dr. Komaroff at Harvard, Dr. Lucinda Batemen in Utah, Dr. Susan Levine and Dr. Derek Enlander in NYC, and until they are proven WRONG, reimburse the WPI for every penny they have invested. they have gotten us MORE press and medical attention in the past 2 years than in the past 20!

Give a round of applause to Dr. Nancy Klimas, Dr. Lenny Jason, Dr. Susan Levine, Dr. Vivian Penn, Dr. Wanda Jones, Dennis Mangan and all the others who tried to make a silk purse out of a sow's ear over the past 2 decades, and congratulate them on their NEW name of the M.E.A.C. the Myalgic Encephalomyelitis Accountability Committee.

Initiate a class action lawsuit against all Long Term Disability companies who have used bad faith, bribery and outright fraud to "delay, deny and hope you die" tens of thousands of very ill people over the past 25 years.

Q: You’ve been very aggressive about putting treatments forward for your patients. How many patients do you currently have on Ampligen, and how many have you treated with Ampligen in total?A: I have 28 people on Ampligen, with a total of 300. With respect to aggressive treatment, for severely disabled patients, and evenly the moderately disabled, unless you introduce some sort of aggressive treatment they don’t spontaneously recover. Symptomatic therapy can be enormously beneficial, but patients don’t recover unless you attack the etiology and pathogenesis directly. We’ve stumbled upon Ampligen, which is very beneficial for a subset of patients.

Q: Vistide (cidofovir) is one of the most difficult drugs to manage. What is your protocol?

A: I have a subset of patients who have evidence of beta herpesvirus reactivation, either CMV or HHV6a or b, and for that subset of patients, particularly if they have it in their spinal fluid, they need a very potent antiviral. For beta herpesviruses we are somewhat limited to a few oral drugs that are not terribly effective, to foscarnet, which is very difficult to administer, and Vistide which is somewhat easier because the infusion is every two weeks. I have treated 65 people according to this protocol, which, relative to the world of chronic fatigue syndrome, is not very many people. But some of those people have had very dramatic responses. Some have been able to go back to work, and to normal lives.

Q: Most doctors do not want to deal with Vistide, isn’t that true?

A: Vistide has to be monitored. You have to monitor kidney function, and liver function, and white blood cell count. I don’t even think it is generally acknowledged that [beta herpesvirus] subsets of these patients are identifiable.Q: Have you used Valcyte?A: I have used Valcyte. I follow the protocol of Jose Montoya at Stanford, with a long course of therapy. It also has to be monitored very carefully, and there are significant side effects such as headache and nausea, etc.

Q: Would you use it again now that you have Vistide?A: I still use it.

Q: From my personal experience [antivirals] do good for a while, then become ineffective. Is that universal?

A: With the herpesviruses, since we never really cure them, patients go into remission and then they relapse. This pattern also holds when patients are treated with Vistide. Most recently, I have been combining therapies, adding immunoglobulin, or Ampligen, or other agents, with some significant success.Q: What is the longest you have been able to keep a patient in good shape?

A: So far, three or four years, but I’m talking about almost total remission. I frequently get asked the question, “Is this curable?” I can’t say that it’s curable, but [the combination of therapies] is able to relieve symptoms so that people can return to work full time, which is pretty dramatic.

Q: Are you looking forward to CMX001 [a lipid antiviral used to boost the effectiveness of Vistide]?

A: Biopharma is great when they see a market, so I look forward to better drugs for all the patients with CFS, not just the subsets with immunological abnormalities. But they are not terribly interested, I think because they don’t recognize the market potential. They can’t get their hands on a biological marker and endpoints. All those things are very important when you are trying to interest pharma. And for a drug that’s already licensed there is no incentive for them to do a study.

Q: Are there any other immune boosters you are interested in?

A: IV gammaglobulin. A new area I’m excited about is the cytokine blockers and the immune modulator rituximab, which has gotten lot of press. Hopefully, they will do a much larger rituximab study in the near future. My concern with rituximab is that I don’t know how to predict who will respond. It would be nice to have guidelines, for entrance criteria, etc. where we could give people an idea of whether or not they will respond. The side effects can be very rough.

Q: If you had all the money in the world, in what direction would you be going now?

A: I would invest the money in centers for excellence. The reason is that primary care physicians can’t manage this disease. It’s too complex, too time-consuming, and they have too many other things to do. If we could get primary care physicians to recognize the disease, to qualify the patient, then they must have some place to refer them to. I see a great need all over the world for people to seek specialty care, which is appropriate until the disease becomes simpler to manage. HIV, for example, has become a very manageable disease. CFS /ME is a long ways from that.

Q: What do we need to do to get there?

A: I think it’s clear this is not a homogeneous disease. I think the CDC is correct in trying to understand subsets and redefine the subsets both biologically and by symptoms. Things would move along more quickly if we did that. As far as a universal definition is concerned, that would be enormously helpful, but we seem to have a great deal of difficulty getting there.Q: Do you see one or two subsets that predominate over the others?A: There seems to a real different between people who have an acute onset versus a gradual onset. About 15% of the people I see have active [viral] infections of one sort or another. They are clearly treatable and should be identified. There are people who have had industrial exposures or heavy metal toxicities, or post-vaccination, or post-transfusion onset. Those are all potentially identifiable subsets that might best be treated differently.Q: Why did chronic fatigue syndrome strike Lake Tahoe? Do you still have people coming in at a high rate?

A: Not locally. The local thing happened and disappeared. Some virus came through this community at that time, striking susceptible people, and then left. I mostly see people from distant places.Q: Who do you need to set up centers for excellence?A: The concept of translational medicine is very good, in which basic researchers work with clinicians – in this disease particularly, where there is not a lot of understanding between the scientists and the clinicians, or pharma for that matter. It would be doable because there are centers of excellence for breast cancer, for MS, for ALS, just go down the list. You can create that model if there is support for it.

Q: Wouldn’t major medical centers be a good place to start, like Stanford and Duke?A: Traditionally, major medical centers have been great sources for centers of excellence. However, they operate very slowly, and they have very high overhead. And funding has been very short term. Some people have started these plans and run out of funds.

Q: As a disease, we get most of our research funding from private funding. Is this an advantage over government funding?A: Private funding is very efficient. It can be targeted and it is easier to obtain in some circumstances. But this is a national problem that should be supported nationally. But I understand that with budget restrictions there is less and less available, particularly of these orphan diseases.Q: Couldn’t the same researchers who do research on MS, or lymphoma, or HIV, be doing research on CFS/ME with very little extra salary?A: That’s a hard sell. It goes back to the stigma of CFS/ME. The name just trivialized the disease. The lack of a clear-cut biological marker held off researchers, as well as short budget cycles, and low dollar amounts. A small grant gets you nowhere with this disease. You need large numbers of patients, which is why I totally support the OMI, with its idea of putting multiple physicians together, and adding all our patients. If you’re talking about things like genomic studies it takes a large number of patients in order to get a sufficient quantity for statistical validity. The same goes for treatment trials. With small treatment trials it’s very difficult to show efficacy.

Q: Is there any way to get researchers to focus on something other than blood? Lymph glands, for example?A: The Ian Lipkin studies at Columbia are looking at other tissues – saliva, urine, cerebrospinal fluid. I think he may be one of the first ones to do that. I am really excited about that research. Hopefully, he will help us in terms of biological markers, or pathogens, and possibly autoimmunity, and chemokine and cytokine signaling. I know he is working on all those avenues. We need people with his kind of expertise and quality to be researchers in this field.

Q: How have you stood it all these years, plugging along in spite of an utter lack of support?

A: That’s a question I get asked frequently. The best answer I can give is that there is still an essential truth that we have to find. Remember, I saw perfectly healthy people become disabled, and nothing can ever convince me that that was not a pathophysiological process. I expected the answer long before now, but I am still looking for answers. The second thing is that discovery comes to the prepared mind. We need intellectual curiosity. We need people asking questions about this, pursuing it. I haven’t seen the end of this story yet, and that’s why I am still in the field.

Web Seminar by Dr. Kenny De Meirleir, March 1, 2013Q: Oxygen Therapy: What Are the Pros and Cons?Administration of oxygen therapy has advantages and disadvantages. Oxygen increases the release of free radicals, which can be harmful. On the other hand oxygen can be very useful for people with severe pain and strong acidification. The oxygen used at home isn’t administered in oxygen cylinders any more. It comes from a device that transforms the air into almost 100% pure oxygen.

Q: Is the oxygen one gets in the hospital the same as your oxygen therapy?

The oxygen one gets from an oxygenator is the equivalent to the oxygen one gets in a hospital.Q: What do you expect from rituximab?

I don’t consider this to be a long-term solution, because practically all patients relapse. A new injection is necessary after six to twelve months, which is extremely expensive. The young and healthy B-cells formed after rituximab treatment will function properly in the beginning, but after a while they will again become involved in the disease process. Therefore rituximab isn’t a definitive solution.Q: Is Ampligen effective? For whom? How does it work?My experience with Ampligen dates from 1992-2001. We gave Ampligen to approximately 150 people during that time. Ampligen partially works like interferon and combats the viral aspect of the disease. So, those ME patients in whom the viral aspect of the disease is dominant will profit most from it.

Q: Are you familiar with fecal transplants? Is this a useful approach?We have heard of some patients who have chosen to have a stool transplant. During the transplant, stool from the intestines is removed and replaced by stool from a healthy individual. I believe this can also provide temporary improvement as fewer toxins are released in the body. But, again, it is not a definitive solution, because the problem isn’t so much the intestines as the immunity of the intestines. The abnormal flora will grow again. In addition, a stool transplant isn’t a pleasant experience, and must be repeated regularly. The only indication for this in ME patients is for those who have an overgrowth of C. difficile, which is extremely toxic, but the same would hold true even for people who don’t have ME.

Q: Can you briefly explain heart-rate monitoring and pacing? What do you expect from these?Several researchers have found that ME patients have irregular heart rhythms. This is due to changes in the sympathetic nervous system, causing inadequate control over heart rhythm. I do think that monitoring can help, but again, this isn’t a treatment of the cause. Pacing helps patients to use less energy. That is, energy is reserved for those things which are essential, in order to make it through the day. Pacing is an alternative for people who are chronically ill and who have few treatment options. They must learn to deal with the amount of energy they have left. Pacing should be addressed when the patient has tried all normal treatments.

Q: Doesn’t long-term administration of antibiotics kill the colonic flora?When one administers broad-spectrum antibiotics for a very long time, then one destroys the colonic flora. But when one is very careful and uses narrow-spectrum antibiotics to treat a specific infection this will not happen. There are numerous examples, as in tuberculosis, in which one administers antibiotics for eighteen months. But treatment involves a narrow-spectrum antibiotic, and therefore the colonic flora aren’t seriously disturbed. In the case of very acute infection one chooses broad-spectrum antibiotics. But when one is going to use long-term antibiotics to combat a very specific intracellular infection one chooses a narrow-spectrum antibiotic that has little effect on the colonic flora.

Just hours before the FDA's April 25th workshop, "Drug Development for Myalgic Encephalomyelitis and Chronic Fatigue Syndrome," Drs. Dan Peterson, Derek Enlander and Nancy Klimas, three CFS/ME specialists with long experience in both treating and researching the illness, held a meeting of their own. Here Cort Johnson reports on what was discussed in that meeting. To read the full report go to the Simmaron website here.

Diagnostics always come first. Before you can treat you must be able to diagnose. Unfortunately the diagnostics in chronic fatigue syndrome have been shrouded, vague, symptom-based definitions. From the myalgic encephalomyelitis to the Holmes to the Fukuda to the Canadian Consensus Criteria, the chronic fatigue syndrome field has been grasping for definitions for as long as it’s been around.

Problems on the macro level (the definition), of course, lead to problems at the micro level ( the doctor’s office) where ME/CFS doctors are deluged with all different kinds of ‘chronic fatigue syndrome’ patients. That uncertainty – not knowing just who might step in the door –surely makes for an interesting job. The qualifications for a good chronic fatigue syndrome physician may look something like this…. good listener, not daunted by complexity, loves to problem-solve, has a wide range of knowledge and is flexible and willing to try new things.

As Bernard Munos pointed out at the FDA Workshop, in a disorder like this, which has few clinical trials, the physicians, more than anyone else are the innovators. Not able to rely on clinical trials, their offices are an ongoing clinical trial.

Given the many different types of patients Dr. Peterson sees, the idea of drug trials that don’t establish subsets first is simply appalling. The idea that this complex mix of patients are ever going to respond similarly to a drug is nonsense.“I am very concerned about random drug trials that take the first 100 patients who sign up. It would be a disaster,” said Dr. Peterson.

For Dr. Peterson, who sees the complexity of the illness daily, diagnosis, whether in a research study, clinical trial or a doctor’s office, always comes first. Since the same symptoms can be produced by many different factors, symptom definitions, while helpful, will always have flaws. What’s needed is to ‘scientifically redefine ME/CFS’; that’s the Simmaron Foundation’s stated goal and each of these physician/researchers is working towards that.

How to Diagnose ME/CFS: The Immune System

Dr. Peterson started off by stating that after screening for the ‘obvious stuff’ he goes after immune markers, primarily focusing on the NK, T and B cells.

Over time he found consistent patterns began to emerge with natural killer (NK) cells playing a major role. (These cells, which play a major role in the early, innate immune response, appear to be ground zero for the immune problems in ME/CFS. Unfortunately, they’re not particularly well known in the medical community. Dr. Peterson’s poll of his colleagues in his area a couple of years ago found that few knew anything about them.)

It doesn’t help that natural killer cells are tricky to work with and need to be assessed within four to six hours of sample collection. In an attempt to make them more user friendly, Dr. Peterson is experimenting with freezing live cells in liquid nitrogen.

As an immunologist, it wasn’t surprising to see Dr. Klimas’ strong focus on the immune system. With one of the top immune labs in the country, Dr. Klimas is at the center of a lot of immunology work on CFS/ME.

Immune factors are one lab measurement that has to be accurate; tweak the powerful immune system the wrong way and you can cause a lot of trouble. If the physician is using immune altering drugs, and both Dr. Peterson and Dr. Klimas do, the ability to trust your lab is critical. Dr. Klimas said her immune lab is the ‘gold standard’ and Dr. Peterson gets all his cytokine arrays done at Dr. Klimas' lab.

Dr. Klimas will dig into IGG subclasses if she sees bacterial infections. Dr. Enlander focuses on much the same factors; CD4 and 8 ratios, NK cells and function, (IL2, IL4, IL10) and uses bacterial cultures to rule out other disease entities, like Lyme, etc.

Pathogens

Pathogens were discussed briefly. All three physicians were testing for them (eg; EBV, HHV6, CMV, Parvovirus, Coxsackie and bacteria), but there were some differences. Dr. Enlander did not see a relationship between viral load and disease severity, something that Dr. Peterson, as we’ll see later, has found, at least with one group of patients. Dr. Klimas has not found HHV6 to be a good marker either, as patients don’t test positive consistently; in fact, she called ME/CFS a ‘good-day, bad-day viral disease’ as patients may test negative on a good day and positive on a bad one. That’s helpful for her as a physician but is not good enough for the FDA to test treatments against. The FDA needs a test that’s consistently positive.

What does Dr. Klimas find that correlates with severity?

Natural killer cell functioning and IL-5 levels might be two markers the FDA could use to assess treatment effectiveness.

We don’t hear a lot about IL-5 but it boosts two immune factors of interest in ME/CFS; mast cells and B-cells. Overactive B-cells have been implicated in autoimmune disorders and, of course, also harbor EBV as well.

Dr. Enlander will be seeking to confirm/deny Dr. Chia’s enterovirus findings in his exercise study.

Autonomic Nervous System

After Dr. Peterson stated that the amount of autonomic nervous system dysfunction in ME/CFS was ‘huge,’ the stage was set for the autonomic discussion. All three doctors do blood pressure and pulse testing. Dr. Peterson and Dr. Enlander do 24-hour BP and heart testing, and Dr. Enlander and Dr. Klimas use tilt table testing. Dr. Klimas noted that autonomic nervous system dysfunction appears to trigger immune dysfunction. She asserted that the sympathetic nervous system is a major player in this disorder and she rattled off problems with standing, respiration, poor digestion, etc. that could all be caused by SNS upregulation.

It’s not clear how many of the physicians were measuring blood volume; it may be that they all simply assume blood volume is low. Dr. Klimas noted the astounding fact that most patients are about a liter of blood low, or about 20% down from normal. With that little blood running through your blood vessels those blood vessels are going to have to squeeze hard to get it out to the tissues and brain, and right there you have a good reason for the sympathetic nervous system activation Dr. Klimas talked about earlier.

Dr. Klimas gives blood volume a boost with electrolytes and then puts the patients back on the tilt table to see if they’ve improved.

Dr. Enlander is using Dr. Cheney’s cardiac protocols to measure cardiac output, stroke volume, etc. He does it, interestingly enough, in a variety of positions (lying down, standing) giving him a great deal of data on cardiovascular functioning.

Aerobic Testing

You probably couldn’t get three ME/CFS physicians more knowledgeable or committed to exercise testing in one room than you had at the Roundtable.

As the first ME/CFS physician to embrace VO2 max testing, Dr. Peterson made a strong plug for Staci Stevens' two-day exercise test protocol (the Stevens Protocol. This exercise test grew out of the work she did in Dr. Peterson’s office).

Dr. Peterson uses the most rigorous test of all; the aerobic exercise test to determine how well his interventions are working. At the FDA Ampligen hearing, Dr. Bateman noted that the VO2 max test, which measures the amount of energy a person can produce, is the hardest to improve of all ME/CFS tests. Since Dr. Peterson finds that low VO2 max scores are often correlated with poor cognition, abnormalities on MRIs and spinal fluid as well as autonomic problems, bumping up those VO2 max scores even moderately can mean a significant improvement in functionality and well-being.

All three practitioners use exercise testing in for research, disability and/or to assess the effectiveness of their interventions

( I asked Staci Stevens if she knew of any ME/CFS patients who had returned to full VO2 max functioning and she said yes, some patients on antivirals and Ampligen had returned to full VO 2 max functioning.)

Dr. Klimas has been digging deep into exercise in her research, which, in turn, is informing her diagnostic work. (This is known as ‘translational medicine’). Earlier this year she reported gene expression studies indicating that the autonomic nervous system drops first during exercise and then drags the immune system down with it.

This major finding, if validated, suggests breakdowns in the ANS, which is tightly intertwined with the immune system, could be at the core of the disorder.

Dr. Enlander is committing a big chunk of money to a sophisticated exercise testing study at the Mt Sinai Research Center. He’s has a geneticist, an immunologist and a pulmonologist all working together.

After having patients exercise, Enlander’s team will be looking at RNA (genes), blood (immune factors, a stool sample, RNA, DNA genome, enteroviruses), brain MRI and SPECT scans. Among other things Enlander will be looking to confirm or deny Dr. Chia’s findings seven years ago of enteroviral infections in CFS/ME patients.Spinal Taps and Brain ImagingDr. Peterson does spinal taps to figure out what’s going on with his most cognitively challenged and neurologically impaired patients. (After decades of gathering spinal fluid, Dr. Peterson easily has the greatest store of ME/CFS spinal fluid on the planet. Dr. Mady Hornig has referred to Dr.Peterson’s spinal fluid as a "precious resource.")

Spinal taps are where Dr. Peterson, Dr. Klimas and Dr. Enlander part ways to some extent. Both Klimas and Enlander do them at times, but Dr. Peterson does them routinely in patients with neurological and brain issues (and he does them himself). Dr. Klimas said she was astounded that Dr. Peterson found 17% of his patients’ spinal fluid tested positive for a virus.Both Drs. Klimas and Enlander may be doing spinal taps more in the future. Dr. Klimas is waiting to find the right neurologist, and Dr. Enlander said he was closely following Peterson’s ideas. If the CFI and PHANU studies using Dr. Peterson’s spinal fluid are positive, we may see more and more doctors turning to spinal fluid to assist with their diagnoses.Dr. Peterson looked forward to future medical advances that will help him fine tune his diagnostic protocols. Genetic technologies are indicating, for instance, that a genetic predisposition to the NK dysfunction may be present in ME/CFS. On the other hand he also finds ‘acquired’ (i.e. non-genetic) NK cell dysfunction as well. He believes insights gathered from mRNA in the spinal fluid of ME/CFS patients, for instance, and more rigorous pathogen detection techniques will continue to open up this field and inform his diagnostics.Similarly, Dr. Klimas’ exercise studies are leading her to focus more on improving autonomic dysfunction in her patients. Dr. Enlander will use his big exercise study to increase his understanding of his patients. Each of these three physician/researchers is eager to incorporate their research findings into their diagnostic protocols.Undefining ME/CFS?“There is an entire school of thought in the medical profession that if anyone with chronic fatigue has anything objectively wrong with them – they don’t have chronic fatigue syndrome.” Dr. Dan PetersonAfter all the talk about how to diagnose ME/CFS, Dr. Peterson brought up a trend towards ‘undefining’ that he found troubling. Undefining ME/CFS consists of putting ME/CFS patients in a different category as soon as something concrete is found. Stating that this attitude is now prevalent, Dr. Peterson explained that a person with ME/CFS with HHV6A in their spinal fluid will be labeled as having HHV6A encephalitis and be determined to never have had ME/CFS.

Dr. Klimas acknowledged that while getting a diagnosis that can be treated is great, culling out large numbers of ME/CFS patients could be devastating. For one, it condemns ‘ME/CFS’ to be a a mere placeholder of an illness.

Dr. Klimas noted that Dr. Peterson’s finding that 17% of his cognitively dysfunctional patients were culture positive for viruses in their spinal fluid comprised a clear subset. (She was reminded of former CDC CFS chief Bill Reeves' response “you don’t know what doesn’t belong there.” She laughed and said, “Wait a minute. Would it be okay for you to have your cognitively dysfunctional child have a positive spinal fluid test? I don’t think so.”) What a dilemma, she said, that every time we start to get clarity, part of this disorder gets shuffled off into another column.The Hidden Epidemic“Talk about a forgotten, ignored group of people.” Dr. PetersonThen there are the missing patients; the bedridden ones who rarely get to doctors' clinics and certainly aren’t in research studies. How do you define a disease without access to all the patients? In most disorders, the most severely ill usually get the most attention, but the opposite is true in ME/CFS. (A former ICU nurse working with Dr. Kogelnik remarked that these patients should be in a hospital, not at home.)Dr. Peterson“The bedridden patients – It’s the hidden epidemic within another epidemic. It’s scary.” Dr. Dan PetersonDr. Peterson noted that we don’t have an accurate count of how many people are in this situation. He didn’t have answers. He noted that you needed staff to get to these people and you needed to find them in the first place. Dr. Klimas suggested that funds were at the heart of the problem. Ads for an online CBT study did bring in bedbound patients who were unable to make it to the clinic, and funding for the ‘good-day/bad-day’study did allow them to make house calls during patients' bad days. Both Dr. Klimas and Dr. Enlander said they do house calls from time to time.

On April 24th, after 22 years of serving as the head of the CFIDS Association of America, Kim McCleary announced her resignation for family reasons. In a touching and, at times, tearful video statement (see below), McCleary stated that her term would be ending in June. McCleary will stay on as an active member of the Association’s Scientific Advisory Board.

McCleary’s term as president and CEO of the CFIDS Association of America began in 1991. During her tenure, McCleary shifted the focus of the organization toward research, policy, and education issues. Her goal was to obtain recognition for ME/CFS as a disabling condition, and to influence policy at the national level.

Under her leadership, the Association played an integral part in developing a policy ruling for the Social Security Administration that recognized CFS as a disabling condition. She fought to create and sustain a dedicated federal advisory committee to the Secretary of Health and Human Services on ME/CFS research and education, and helped expose the misappropriation of $12.9 million in CDC spending, restoring these funds to ME/CFS research. McCleary led the first-ever public awareness campaign for ME/CFS, led lobbying events, organized Congressional briefings and delivered testimony at numerous federal hearings and meetings.

McCleary’s strong personal attachment to the ME/CFS community was evident during her resignation speech, during which she listed the accomplishments of the Association, and expressed her commitment to create a world without ME/CFS. In a voice choked with emotion, she lauded the struggles of “family members, parents, spouses, brothers, sisters, sons, daughters who resolve to battle for their loved ones, and all people affected by ME/CFS.” Through tears, McCleary said, “I look forward to watching progress in the days ahead and to celebrating with you when effective treatments and cures return every person living with ME/CFS to lives they dream of living again.” We look forward to that day as well, and, when it comes, we hope to celebrate it with Kim McCleary.

Transcript

“Hi, I’m Kim McCleary president and CEO of the CFIDS Association of America. In 1991 I joined the CFIDS Association and this community as the organization’s first chief staff executive. When I came to this organization, I could not have envisioned all the ways in which my work would become my life and how the people I would meet would shape and redefine me. I’ve been honored to partner with thousands of volunteers, nearly a hundred board members, fifty staff members, seven chairmen, and founder, Mark Iverson, to advance our mission. I will always be a vocal champion for this organization and its vision of a world without ME/CFS. Over the past 22 years I have been part of some incredible work, the drug development and patient focus workshop that FDA will host later this week, launching the world’s first patient-centered virtual institute for ME/CFS, the Research Institute Without Walls, and dozens of events, live and over the web that gave voice to thousands of people with ME/CFS.I’ve come to know some of these amazing people personally. People who face this uncertain, chronic, debilitating condition with a brand of courage and optimism I don’t think I could muster or sustain: family members, parents, spouses, brothers, sisters, sons, daughters, who resolve to battle for their loved ones, and all people affected by ME/CFS. Each and every person I’ve met through the vital work of this organization has touched my life in ways I’ll carry with me lifelong. Along with my family I will be relocating in June, and it is time to write a new chapter. The vision is clear. The path is laid out before us. Over the past several months the leadership team has worked together to develop an incredibly strong strategic plan that is already changing the landscape for ME/CFS research to accelerate the path for safe and effective treatments. There is an amazing team in place that will execute that plan and make it reality for you. I pledge my continued dedication through the end of my term in June, and then I will proudly serve as an active member of the Association’s Scientific Advisory Board, so that our work together will not end.My personal connection to this community will endure and leave a lasting impression on my life. I humbly thank you for the years you have entrusted me to steward this fine organization. I look forward to watching progress in the days ahead and to celebrating with you when effective treatments and cures return every person living with ME/CFS to lives they dream of living again."

Dr. Kenny De Meirleir spoke at the Whittemore Peterson Institute on January 28, 2013. The following summary of his talk was posted on January 30 on WPI's blog, Wings of Hope.

Dr. Vincent Lombardi, WPI Research Director, introduced Dr. De Meirleir as one of the world's foremost experts in ME and primary research collaborator on WPI’s current RO1 federal grant. He also stated that Dr. De Meirleir has authored hundreds of publications and several books on ME/CFS and other medical research topics. Dr. Daniel Peterson, who was in the audience, was also recognized for his outstanding contributions to this field of medicine.

Dr. De Meirleir's talk included years of significant research which is very technical and complicated. Therefore, this review is not meant to be a summary of the underlying science but rather a summary of the practical application of this work. However, we will place a recording of this talk on the WPI website: www.wpinstitute.org, as soon as possible for those who are interested in the actual research data.

Dr. De Meirleir presented a comprehensive lecture on the many factors that appear to play a role in the pathophysiology of ME. In support of his conclusions, he drew information from other well-known researchers in the field including Drs. Chia, Klimas, Peterson, Mella and Fluge, as well as his more recent clinical studies of patients from Belgium and Norway. After the one hour and fifteen minute presentation, interested patients, researchers, doctors, nurses, and medical students were given a chance to ask questions.

Dr. De Meirleir uses a number of diagnostic tests to diagnose his patients’ underlying biological abnormalities and to guide his successful treatment protocols. Biomarkers include abnormally low NK cell number and function, cytokines indicating a shift in the balance of Th1 and Th2 immune responses, up regulation of Th17 immune cells, and abnormal levels of nagalase and elastase activity. He also tests for various active infectious agents including Borrelia, Bartonella, Brucella, mycoplasma, parasites, and various herpes viruses. He stated that environmental and genetic factors contribute to aberrant protein conformation in some patients. Other diagnostic tests include fecal analysis and tests for levels of LPS or soluble CD14 as an indicator of gut inflammation. Basic to Dr. De Meirleir’s treatment protocol is a plan that addresses specific dietary restrictions. He reported that many patients are fructose, lactose, casein and/or gluten intolerant. His patients often begin feeling better after eating a diet free of these substances, as they are most likely to cause an inflammatory response. In addition, he includes a fecal microbial analysis to determine whether or not to begin treatment with pulsed antibiotics. Based on the fecal analysis, which indicates whether or not his patients are suffering from a compromised intestinal barrier, he also prescribes specific probiotics, prebiotics such as lactoferrin, and digestive enzymes. When viruses or other pathogens become chronic Dr. De Meirleir prescribes antiviral therapies and/or additional antibiotic treatments.

It is generally accepted knowledge that ME patients have difficulty controlling various herpes viruses and other pathogens, in addition to exhibiting abnormal natural killer cell function. Subsequent searches for immune modulating drugs have included trials of several different products. Gc-MAF is a macrophage stimulating substance that has recently shown great promise. Dr. De Meirleir highly recommends that patients address any leaky gut issues before beginning treatment with Gc-MAF. He also mentioned risks that can be associated with this type of treatment. Risks include a shift to autoimmunity and an immune reconstitution reaction known as IRIS although none of his patients have developed autoimmune disease as a result of Gc-MAF treatments and less than 20% have experienced IRIS. Dr. De Meirleir routinely monitors his patients for IRIS cytokines after starting them on very low doses of Gc-MAF, as a method of prevention. Other immune supportive therapies include the use of Kutapression/Hepapressin complex (Nexavir), which has been reported to inhibit EBV and HHV-6, and Isoprinosine for those with low serum uric acid levels. Finally, Rituximab, a B-cell depletion immune therapy, has been used successfully in a small trial of patients with ME by oncologists Fluge and Mella. Because of the delayed therapeutic response of two to seven months, the authors of this study remarked that there is a possibility that ME has an autoimmune component. (Note: These two physicians are now looking for collaborative research sites and additional funding to engage in a much larger clinical trial due to their 67% rate of success.) Dr. De Meirleir concluded his talk with a detailed slide describing the various pathways that are disrupted in ME and several other autoimmune diseases. He spoke about a continuum of autoimmune diseases including ME, lupus, RA, type 1 diabetes, and remitting MS that involve a dysregulation of two important immunological pathways, 2’-5’OA synthetase and Th1/Th2 immunity. It was evident from his lecture that the key to Dr. De Meirleir’s success with patients is his recognition of the serious infectious and immunological issues facing those with ME. His research provides strong evidence for the support of biological testing and treatment. WPI is thankful to Dr. De Meirleir for his outstanding commitment to this patient population. We feel fortunate to be able to provide his lecture as part of our mission to support outreach and education. We look forward to sharing more good news with you in the future.

Dr. Lucinda Bateman is an internist specializing in the treatment of CFS/ME. She is a graduate of the Johns Hopkins School of Medicine. Dr. Bateman interned at the University of Utah for Internal Medicine and became certified by the American Board of Internal Medicine in 1991. Until 2000, when she opened her Fatigue Consultation Clinic, she practiced as a general internist.

Dr. Bateman's interest in CFS/ME began when she moved back to Utah in 1987 to begin her residency. Her older sister, Shauna Bateman Horne, had become chronically ill with a mysterious malady. The doctors were unable to diagnose her and came to the conclusion that she was suffering from depression. Their treatment recommendation was that she “take a night class.” Dr. Bateman suspected there was more going on and began investigating fibromyalgia and CFS/ME as possible causes of her sister's illness. In 2000, Shauna was diagnosed with Non-Hodgkins lymphoma and died from complications of a stem cell transplant in May of 2001. Dr. Bateman has served on the boards of the International Association of Chronic Fatigue Syndrome (IACFS/ME) and the CFIDS Association of America. Dr. Bateman is also the co-founder and a board member of OFFER (the Organization for Fatigue and Fibromyalgia Education and Research). Since opening her Fatigue Consultation Clinic in 2000, Dr. Bateman has evaluated more than 1000 patients.

Author

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About me:I'm a 25-year veteran of CFIDS. I know what it is like to be bedbound for long stretches of time. I also know what it is like to recover, and to relapse. But this blog is not about my personal experience. It is intended to be a resource - a collection of anything that might be helpful to the CFIDS community: book reviews, advice, CFIDS news, research, advocacy, opinion, who's who in our community, fundraising... and occasionally a bit of humor.

Disclaimer: I am not a doctor, which means nothing I write, no matter how sensible it may be, should be interpreted as medical advice.